Studies of the B19 parvovirus have utilized a suspension culture system for propogration of the virus for detailed molecular analysis of virus replication, transcription, and protein synthesis. B19 parvovirus DNA replication is similar to that of other parvoviruses, proceeding through double-stranded high molecular weight intermediate forms. B19 parvovirus proteins are also similar to those of other parvoviruses, consisting of two capsid proteins of 58 and 83 kd and at least one nonstructural protein of 77 kd. In contrast to other parvoviruses, the transcription map of the B19 parvovirus is extraordinarily complex, and detailed analysis has shown that regulation, independent of promoter strength, likely results from differential splicing or transcription termination. Specific virus protein products have been assigned to RNA species, and viral proteins translated in vitro. A cytotoxic function has been assigned to the nonstructural protein using transfection of recombinant constructs into HeLa cells. In clinical studies, the spectrum of parvovirus disease has been expanded by the description of the first case of persistent B19 infection, in a child with congenital immunodeficiency, result in chronic bone marrow failure. The normal host defense to B19 parvovirus infection appears to be predominantly humoral and mediated by neutralizing antibodies. B19 parvovirus has been detected in the circulating cells of patients acutely infected and may be present in granulocyte precursors. In parallel studies of feline panleukopenia virus, a common natural cause of neutropenia and aplastic anemia in cats, virus replication and propagation have been detected in vitro using bone marrow cultures and shown to be dependent upon the addition of hematopoietic colony stimulating factors. Feline panleukopenia virus is a potent inhibitor of colony formation by cat progenitor cells from all lineages.